No abstract available.
Rupture* ; Spleen*

No abstract available.
Cicatrix* ; Contracture* ; Forearm* ; Hand*

The nerve root block or selective nerve root block is one of the primarily preoperative diagnostic tool to identify and confirm the lesion site of primary cause of pain and that is considered as one component of a comprehensive treatment program. The purpose of our study is to evaluate the effect and duration of the pain control by selective spinal nerve root block as a conservative treatment in patients presenting with chronic or recurrent sciatica. The authors performed 95 selective nerve root blocks in 72 patients from Sep. 1994 to May. 1996, (mean follow up 11.6 month) at the department of orthopedic surgery, Kosin University Gospel Hospital, and the results were as follows: 1. Among 72 cases, spinal stenosis was in 45 cases (62.5%), HIVD in 19 cases (26.4%), failed back syndrome in 5 cases (6.9%), spondylosis in 2 cases (2.8%), and spondylolisthesis in I case (1.4%). 2. In 72 cases, improved more than 50% of sciatica were 61 cases (84.7%) at 3 hours, 53 cases (73.6%) at I week, 35 cases (48.6%) at 1 month, 33 cases (45.8%) at 3 months, and 33 cases (45.8%) at 6 months respectively. 3. At last follow-up, excellent and good results were 35 cases (48.6%), fair results were 25 cases (34.7%) and poor results were 12 cases (16.7%) by the Kirkaldy-Willis criteria. 4. Complications were 1 case of transient hypotension, 2 cases of severe paresthesia, but subsided without residual complication. Therefore, the selective nerve root block is one of the valuable procedure that is helpful and extremely safe in useful treatment for radicular pain associated with lumbar disease. And the trial of selective nerve root block was recommended before deciding surgical intervention on an outpatient basis.
Follow-Up Studies ; Humans ; Hypotension ; Orthopedics ; Outpatients ; Paresthesia ; Sciatica* ; Spinal Nerve Roots* ; Spinal Nerves* ; Spinal Stenosis ; Spondylolisthesis ; Spondylosis

No abstract available.
Cicatrix* ; Contracture* ; Forearm* ; Hand*

We present a case of acquired tracheoesophageal fistula (TEF) which was found during induction of general anesthesia for clipping of aneurysm. The patient had been intubated with endotracheal tube for 10 days and then done tracheotomy for 45 days. Thereafter, TEF was confirmed by MRI and treated with fistula repair and tracheal fenestration. Acquired TEF can occur under the condition of prolonged tracheal intubation with high cuff pressure (>30 mmHg) and can also result from intratracheal neoplasm, mediastinitis, and other tracheal or esophageal damages. If unrecognized during anesthetic induction, TEF can cause gastric dilatation and rupture, pulmonary aspiration and respiratory failure. So early diagnosis and proper management is very important whenever TEF is suspected during anesthetic induction.
Anesthesia, General ; Aneurysm ; Early Diagnosis ; Fistula ; Gastric Dilatation ; Humans ; Intubation ; Magnetic Resonance Imaging ; Mediastinitis ; Respiratory Insufficiency ; Rupture ; Tracheoesophageal Fistula* ; Tracheotomy

The placenta is a temporary fetomaternal organ capable of supporting fetal growth and development during pregnancy. In particular, abnormal development and dysfunction of the placenta due to cha nges in the proliferation, differentiation, cell death, and invasion of trophoblasts induce several gynecological diseases as well as abnormal fetal development. Autophagy is a catalytic process that maintains cellular structures by recycling building blocks derived from damaged microorganelles or proteins resulting from digestion in lysosomes. Additionally, autophagy is necessary to maintain homeostasis during cellular growth, development, and differentiation, and to protect cells from nutritional deficiencies or factors related to metabolism inhibition. Induced autophagy by various environmental factors has a dual role: it facilitates cellular survival in normal conditions, but the cascade of cellular death is accelerated by over-activated autophagy. Therefore, cellular death by autophagy has been known as programmed cell death type II. Autophagy causes or inhibits cellular death via the other mechanism, apoptosis, which is programmed cell death type I. Recently, it has been reported that autophagy increases in placenta-related obstetrical diseases such as preeclampsia and intrauterine growth retardation, although the mechanisms are still unclear. In particular, abnormal autophagic mechanisms prevent trophoblast invasion and inhibit trophoblast functions. Therefore, the objectives of this review are to examine the characteristics and functions of autophagy and to investigate the role of autophagy in the placenta and the trophoblast as a regulator of cell death.
Apoptosis ; Autophagy* ; Cell Death* ; Cell Differentiation ; Cellular Structures ; Digestion ; Fetal Development ; Fetal Growth Retardation ; Homeostasis ; Lysosomes ; Malnutrition ; Metabolism ; Placenta* ; Pre-Eclampsia ; Pregnancy ; Recycling ; Trophoblasts

No abstract available.
Idiopathic Pulmonary Fibrosis*

Laminin-1 is biologically active and can effect cellular proliferation, differentiation, migration, and apoptosis. In the central nervous system, neuronal cells are rarely reported to give positive reaction by laminin antibody staining. However, the original cell type which can produce the laminin molecule has not been well established. Since the neuronal cells of brain are derived from neuroectoderm, we thought that the neuronal cells should be able to produce the laminin molecules as other epithelial cells. In this study we aimed to explore whether the neuronal cells express the laminin chain mRNAs, and further to identify which types of laminin isoform are expressed at the specific sites of the brain structure. We found that neuronal cell was the important cell type in mouse brain, which could produce laminin isoforms. Although immunostainings disclosed reactivity of laminins in the basement membrane of capillaries as well as neuronal cells, mRNA expressions of laminins were intense only in the neuronal cells. It was relatively weak in the endothelial cells. Among neuronal cells the cortical cells of cerebrum, pyramidal cells of hippocampus, and Purkinje cells of cerebellum showed pronounced expression of laminin chain mRNA. Glial cells, especially astrocytes, were negative for laminin subtypes both in immunohistochemistry and in situ hybridization. Taken together, our data indicate that the neuronal cells of mouse brain actively produce laminin isoforms, and the resultant polymerized laminins are accumulated mainly in the basement membrane of capillaries. In conclusion, the results indicate that neuronal cells produce and utilize the different laminin chains to maintain the neurovascular environment of brain.
Animals ; Apoptosis ; Astrocytes ; Basement Membrane ; Brain* ; Capillaries ; Cell Proliferation ; Central Nervous System ; Cerebellum ; Cerebrum ; Endothelial Cells ; Epithelial Cells ; Hippocampus ; Immunohistochemistry ; In Situ Hybridization ; Laminin* ; Mice* ; Neural Plate ; Neuroglia ; Neurons* ; Polymers ; Protein Isoforms ; Purkinje Cells ; Pyramidal Cells ; RNA, Messenger

No abstract available.
Mandible* ; Osteoblastoma*

No abstract available.
Mandible* ; Osteoblastoma*